Mitochondrial electron transport chain is involved in microcystin-RR induced tobacco BY-2 cells apoptosis  

作　　者：Wenmin Huang Dunhai Li Yongding Liu 

机构地区：[1]Key Laboratory of Algal Biology,Institute of Hydrobiology,Chinese Academy of Sciences [2]Key Laboratory of Aquatic Botany and Watershed Ecology,Wuhan Botanical Garden,the Chinese Academy of Sciences

出　　处：《Journal of Environmental Sciences》2014年第9期1930-1935,共6页环境科学学报（英文版）

基　　金：supported by the National Natural Science Foundation of China (No.31100340);the Major Science and Technology Program for Water Pollution Control and Treatment (No.2012ZX07103-004-02)

摘　　要：Microcystin-RR （MC-RR） has been suggested to induce apoptosis in tobacco BY-2 cells through mitochondrial dysfunction including the loss of mitochondrial membrane potential . TO further elucidate the mechanisms involved in MC-RR induced apoptosis in tobacco BY-2 cells, we have investigated the role of mitochondrial electron transport chain （ETC） as a potential source for reactive oxygen species （ROS）. Tobacco BY-2 cells after exposure to MC-RR （60 mg/L） displayed apoptotic changes in association with an increased production of ROS and loss of Am. All of these adverse effects were significantly attenuated by ETC inhibitors including Rotenone （2 μmol/L, complex I inhibitor） and antimycin A （0.01 μmol/L, complex III inhibitor）, but not by thenoyltrifluoroacetone （S μmol/L, complex Ⅱinhibitor）. These results suggest that rnitochondrial ETC plays a key role in mediating MC-RR induced apoptosis in tobacco BY-2 cells through an increased mitochondrial production of ROS.Microcystin-RR （MC-RR） has been suggested to induce apoptosis in tobacco BY-2 cells through mitochondrial dysfunction including the loss of mitochondrial membrane potential . TO further elucidate the mechanisms involved in MC-RR induced apoptosis in tobacco BY-2 cells, we have investigated the role of mitochondrial electron transport chain （ETC） as a potential source for reactive oxygen species （ROS）. Tobacco BY-2 cells after exposure to MC-RR （60 mg/L） displayed apoptotic changes in association with an increased production of ROS and loss of Am. All of these adverse effects were significantly attenuated by ETC inhibitors including Rotenone （2 μmol/L, complex I inhibitor） and antimycin A （0.01 μmol/L, complex III inhibitor）, but not by thenoyltrifluoroacetone （S μmol/L, complex Ⅱinhibitor）. These results suggest that rnitochondrial ETC plays a key role in mediating MC-RR induced apoptosis in tobacco BY-2 cells through an increased mitochondrial production of ROS.

关 键 词：Microcystin-RRTobacco BY-2 cellsApoptosisReactive oxygen speciesMitochondrial electron transport chain 

分 类 号：X173[环境科学与工程—环境科学]